Hypothesis: In our lab, we have found that reperfusion injury produces a phenotype in the injured tissue that then invites self-attack by natural antibody and the classical pathway of complement. Our investigations to date indicate that a single clone of natural IgM initiates reperfusion injury in antibody-deficient mice. As we have tested additional IgM clones that do not have this property, we hypothesize that this particular IgM binds to a specific ligand in ischemic tissue. In another model of injury, burns, we have found that the same agents that modify reperfusion injury also modify burn wounds indicating either that there is an element of reperfusion injury in burn wounds or that the two different injuries are amplified by a mechanism common to many types of injury. Aim A. To test whether the murine B1 cell hybridoma-derived IgM that initiates reperfusion injury ("CM22") binds to specific cell antigens. A.1. To test whether CM22 binds specifically to burn murine tissue. A.2. To test whether CM22 binds specifically to an identifiable murine tissue antigen ("CM22AG"). [unreadable] [unreadable] [unreadable]